The long-term goal of this proposal is to elucidate the neural circuit level properties and mechanisms which underlie the immediate and pronounced reorganization of sensory maps in the somatosensory system caused by local anesthesia of the face. The basic hypothesis is that sensory representations in the somatosensory system are not "hard wired", but, instead, represent a "dynamic equilibrium" between both feedforward and feedback influences on sensory processing neurons. This hypothesis predicts that inactivation of any particular part of this system should cause rapid and compensatory changes throughout much of the rest of the system. The specific aims of this proposal are to characterize the role of the somatosensory cortex (S1), the posterior medial nucleus of the thalamus (P0m), and the spinal trigeminal (interpolaris) nucleus (SpV) in the reorganization of somatotopic maps caused by peripheral anesthesia. These goals will be accomplished by recording single unit activity of many neurons simultaneously through arrays of microwire electrodes implanted at multiple levels of the trigeminal sensory pathway of rats while either S1, POm, or SpV is reversibly inactivated by focal micro-injections of the GABA-A agonist muscimol. Quantitative measurement of the receptive fields of each neuron as well as "population maps" will be determined prior to focal inactivations. These same measures will be repeated during the inactivations and again following recovery. These measurements will allow precise quantitative determination of the time course of induced changes in sensory representations resulting from these inactivations. These results will provide further insight into our understanding of not only how the brain processes information normally but how the brain recovers from injury, an understanding which is crucial for developing improved means of treating such injuries.